Circulating acyl and des-acyl ghrelin levels in obese adults: a systematic review and meta-analysis

Ghrelin is the only known orexigenic gut hormone, and its synthesis, secretion and degradation are affected by different metabolic statuses. This meta-analysis aimed to investigate the potential differences in plasma acyl ghrelin (AG) and des-acyl ghrelin (DAG) concentrations between normal weight and obese adults. Systematic literature searches of PubMed, Embase and Web of Science through October 2021 were conducted for articles reporting AG or DAG levels in obesity and normal weight, and 34 studies with 1863 participants who met the eligibility criteria were identified. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated to evaluate group differences in circulating AG and DAG levels. Pooled effect size showed significantly lower levels of baseline AG (SMD: − 0.85; 95% CI: − 1.13 to − 0.57; P SMD < 0.001) and DAG (SMD: − 1.06; 95% CI: − 1.43 to − 0.69; P SMD < 0.001) in obese groups compared with healthy controls, and similar results were observed when subgroup analyses were stratified by the assay technique or storage procedure. Postprandial AG levels in obese subjects were significantly lower than those in controls when stratified by different time points (SMD 30 min : − 0.85, 95% CI: − 1.18 to − 0.53, P SMD < 0.001; SMD 60 min : − 1.00, 95% CI: − 1.37 to − 0.63, P SMD < 0.001; SMD 120 min : − 1.21, 95% CI: − 1.59 to − 0.83, P SMD < 0.001). In healthy subjects, a postprandial decline in AG was observed at 120 min (SMD: − 0.42; 95% CI: − 0.77 to − 0.06; P SMD = 0.021) but not in obese subjects (SMD: − 0.28; 95% CI: − 0.60 to 0.03; P SMD = 0.074). The mean change in AG concentration was similar in both the obese and lean health groups at each time point (ΔSMD 30min : 0.31, 95% CI: − 0.35 to 0.97, P SMD = 0.359; ΔSMD 60min : 0.17, 95% CI: − 0.12 to 0.46, P SMD = 0.246; ΔSMD 120min : 0.21, 95% CI: − 0.13 to 0.54, P SMD = 0.224). This meta-analysis strengthens the clinical evidence supporting the following: lower baseline levels of circulating AG and DAG in obese individuals; declines in postprandial circulating AG levels, both for the healthy and obese individuals; a shorter duration of AG suppression in obese subjects after meal intake. These conclusions have significance for follow-up studies to elucidate the role of various ghrelin forms in energy homeostasis.